1. ¹Center for Diabetes and Cardiovascular Health, University of Missouri, Columbia, Missouri, USA
2. ²University of Missouri School of Medicine, VA Medical Center, Columbia, Missouri, USA

Correspondence: Dr. James R. Sowers, MA410 Medical Science Building, One Hospital Drive DC043.00, Columbia, MO 65212 E-mail: Sowersj@health.missouri.edu

Received 30  2004; Accepted 1  2004.

Abstract

The major cause of morbidity and mortality in persons with diabetes is cardiovascular disease (CVD), the risk of which is increased three- to four-fold versus persons without diabetes. The biology of diabetes is characterized not only by hyperglycemia but also by hypertension, dyslipidemia, microalbuminuria, inflammation, and abnormal thrombolysis. Hypertension is a common feature of diabetes and is the primary contributor to CVD. Recent investigations have revealed a relationship between vascular derangements, insulin resistance, and visceral obesity and have implicated the renin-angiotensin-aldosterone system (RAAS) as a key mediator of cardiovascular dysfunction in diabetes. Angiotensin II has been shown to have direct effects on endothelial dysfunction, oxidative stress, inflammation, skeletal muscle, and adipocyte function. These pathophysiologic considerations have formed the basis for CVD prevention strategies in diabetes. Clinical trials have demonstrated a reduction in cardiovascular events with aspirin, lipid-lowering agents, and antihypertensive agents. Blood pressure (BP) control (<130/80 mm Hg) is a crucial component of risk reduction, and several studies have demonstrated the need for multiple agents to reach therapeutic goals. Clinical trials also demonstrated the benefit of RAAS blocking agents in reducing BP and cardiovascular and renal risk, and suggest clinical benefits beyond BP reduction.